Hemodynamic Parameters and Early Intimal Thickening in Branching Blood Vessels

Abstract

Intimal thickening due to atherosclerotic lesions or intimal hyperplasia in medium to large blood vessels is a major contributor to heart disease, the leading cause of death in the Western World. Balloon angioplasty with stenting, bypass surgery, and endarterectomy (with or without patch reconstruction) are some of the techniques currently applied to occluded blood vessels. On the basis of the preponderance of clinical evidence that disturbed flow patterns play a key role in the onset and progression of atherosclerosis and intimal hyperplasia, it is of interest to analyze suitable hemodynamic wall parameters that indicate susceptible sites of intimal thickening and/or favorable conditions for thrombi formation. These parameters, based on the wall shear stress, wall pressure, or particle deposition, are applied to interpret experimental/clinical observations of intimal thickening. Utilizing the parameters as "indicator" functions, internal branching blood vessel geometries are analyzed and possibly altered for different purposes: early detection of possibly highly stenosed vessel segments, prediction of future disease progression, and vessel redesign to potentially improve long-term patency rates. At the present time, the focus is on the identification of susceptible sites in branching blood vessels and their subsequent redesign, employing hemodynamic wall parameters. Specifically, the time-averaged wall shear stress (WSS), its spatial gradient (WSSG), the oscillatory shear index (OSI), and the wall shear stress angle gradient (WSSAG) are compared with experimental data for an aortoceliac junction. Then, the OSI, wall particle density (WPD), and WSSAG are segmentally averaged for different carotid artery bifurcations and compared with clinical data of intimal thickening. The third branching blood vessel under consideration is the graft-to-vein anastomosis of a vascular access graft Suggested redesigns reduce several hemodynamic parameters (i.e., the WSSG, WSSAG, and normal pressure gradient [NPG]), thereby reducing the likelihood of restenosis, especially near the critical toe region.

Morphometric and hemodynamic analysis of atherosclerotic progression in human carotid artery bifurcations

“…The ECA diameter in patients with carotid artery disease was significantly reduced (P Ͻ 0.05), while the CCA diameter was not statistically different from the control (P ϭ 0.18). Moreover, Patients [25][26][27][28][29][30] in Table 4, who were the youngest (ages 40 Ϯ 6 yr) and had extension of stenosis to the entire cervical ICA, showed smaller diameters of CCA and ECA than Patients [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] (ages 54 Ϯ 12 yr) with no stenoses in the distal regions of ICA. Patients 19 -24 in Table 4, who were the oldest (ages 71 Ϯ 7 yr) and had extension of stenosis to the middle of cervical ICA, showed larger angle 2 than Patients 1-18 and Patients [25][26][27][28][29][30] despite the lack of significant difference of angle 1.…”

“…3, A-C, show the variation of D fit along normalized ICA center lines with the stenosis near bifurcation (Patients [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] ) and in the middle of the vessel (Patients 19 -24 ) and with extension to the entire vessel (Patients [25][26][27][28][29][30] ), respectively. The black line, "control," represents the mean value of D fit (averaged over all controls) and error bars refer to SD.…”

“…Atherosclerotic plaques usually reside in artery bifurcations with complex flow patterns (6,7,10,13,15,17). Because of its clinical relevance to stroke (9), the morphometry of human carotid artery bifurcation [comprised of the left and right common (CCA), internal (ICA), and external (ECA) carotid arteries] (16) has received intensive investigation (3,23,24,27).…”

Hypoxia: The Force that Drives Chronic Kidney Disease

“…The advanced lesions of atherosclerosis compromise the lumen diameter, reducing the blood flow in arteries and thus limiting kidney oxygenation. [44][45][46][49][50][51][52] In the early stages of atherosclerotic renal artery stenosis progressive decreases in blood flow are accompanied by compensatory changes in arteriovenous shunting, and decreases in glomerular filtration rate and tubular reabsorption of sodium, that either increase oxygen availability or reduce its consumption. Within the whole kidney these adaptive mechanisms appear to maintain appropriate oxygenation.…”

“…This in turn is driven by a constellation of interlinked risk factors. Primary amongst these factors are anemia, [6][7][8][9] diabetic hyperglycemia, [10][11][12] hypertension, [13][14][15][16][17] hypercholesterolemia, [18][19][20] cigarette smoking, [21][22][23][24][25][26][27] air pollution, [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] atherosclerosis, [43][44][45][46][47][48][49][50][51][52] repeated episodes of acute kidney injury, [53][54][55][56]…”